The authors regret having incorrectly written in equation (7) that the fraction of surviving cells (SF) is obtained using the natural logarithm of the negative value of the number of lethal lesions L_f. The natural logarithm must be replaced by the exponential function as follows: [Formula presented] Although the equation is incorrectly written in the paper, its correct expression has been used in the results of the analysis shown in Figure 4. This error has no impact on the other results and conclusions of the paper. The authors would like to apologise for any inconvenience caused.

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The authors regret having incorrectly written in equation (7) that the fraction of surviving cells (SF) is obtained using the natural logarithm of the negative value of the number of lethal lesions Lf. The natural logarithm must be replaced by the exponential function as follows: [Formula presented] Although the equation is incorrectly written in the paper, its correct expression has been used in the results of the analysis shown in Figure 4. This error has no impact on the other results and conclusions of the paper. The authors would like to apologise for any inconvenience caused.
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Purpose: Track structure Monte Carlo (MC) codes have achieved successful outcomes in the quantitative investigation of radiation-induced initial DNA damage. The aim of the present study is to extend a Geant4-DNA radiobiological application by incorporating a feature allowing for the prediction of DNA rejoining kinetics and corresponding cell surviving fraction along time after irradiation, for a Chinese hamster V79 cell line, which is one of the most popular and widely investigated cell lines in radiobiology. Methods: We implemented the Two-Lesion Kinetics (TLK) model, originally proposed by Stewart, which allows for simulations to calculate residual DNA damage and surviving fraction along time via the number of initial DNA damage and its complexity as inputs. Results: By optimizing the model parameters of the TLK model in accordance to the experimental data on V79, we were able to predict both DNA rejoining kinetics at low linear energy transfers (LET) and cell surviving fraction. Conclusion: This is the first study to demonstrate the implementation of both the cell surviving fraction and the DNA rejoining kinetics with the estimated initial DNA damage, in a realistic cell geometrical model simulated by full track structure MC simulations at DNA level and for various LET. These simulation and model make the link between mechanistic physical/chemical damage processes and these two specific biological endpoints.

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The advancement of multidisciplinary research fields dealing with ionising radiation induced biological damage – radiobiology, radiation physics, radiation protection and, in particular, medical physics – requires a clear mechanistic understanding of how cellular damage is induced by ionising radiation. Monte Carlo (MC) simulations provide a promising approach for the mechanistic simulation of radiation transport and radiation chemistry, towards the in silico simulation of early biological damage. We have recently developed a fully integrated MC simulation that calculates early single strand breaks (SSBs) and double strand breaks (DSBs) in a fractal chromatin based human cell nucleus model. The results of this simulation are almost equivalent to past MC simulations when considering direct/indirect strand break fraction, DSB yields and fragment distribution. The simulation results agree with experimental data on DSB yields within 13.6% on average and fragment distributions agree within an average of 34.8%.

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